Saturday, February 20, 2021

Jimmy Increased Urination Out of the Box, Increased Glucose Levels, Increased Blood in Urine, Hypercobalaminaemia

April 2020: End of April, Jimmy went out of the litter box in various areas of the house. So, he saw the vet for blood work and an ultrasound and some possible issues emerged. He possibly has: prediabetes, pancreatitis, liver disease, early kidney disease. Here's a review of his history and test results. At the end, I will list what steps we are taking.

Brief history: he's on Prozac for litter box use since 2010 which worked perfectly. He did have incidences about four times a year but on pads near the boxes. The prozac stopped the random spraying. But then the incidences began again about 2014. Testing showed he was prediabetic when his glucose level shot up to 320 (175 is high normal) and the fructosamine test was high, and he had glucose in the urine (should not be present in the urine at all.) Glucose in the urine creates the feeling of a full bladder, can create an irritation in the bladder, and cause the cat to want to suddenly, to urinate anywhere possible. We changed his diet to a lower carb diet-a pate, as the gravy version was high in carbs (to make the gravy) and carbs add to glucose.  This diet change was enough to bring down his glucose levels, and improve his furctosamine levels, and he has not had glucose in his urine.

This decreased the random urination until 2016 when a new cat Roxanne came into the house. Increasing the dosage of the Prozac helped but didn't stop the incidences. He began to go out of the box at least once a month. It seemed like clock work. I could not stop it-was he getting into dry food (too many carbs); was he eating other food fed to other cats that he shouldn't; was he eating too much or too little-did it effect his glucose levels; was it the herpes virus? We tried soothing supplements-Solequin, and another one I cannot recall BUT they seemed to make the problem WORSE and I think it was because they interfered with the Prozac. We tried spraying Felaway calming spray which helped but did not stop the incidences. By 2019, signs of possible kidney issues emerged in the blood work. A scan showed possible changes in the kidneys. Taking him off of Solequin and other supplements that interfered with Prozac, and increasing the dosage of Prozac helped but did not stop the urinating out of the box. He has for two years, gone at least once a month out of the box, typically on pads near the boxes. But he began going 2-3 times a month in other places since January. 

End of April, Jimmy went out of the litter box in various areas of the house three times in two weeks. 
So, he saw the vet for blood work and an ultrasound and some possible issues emerged.

In his urine:
He had urine protein at 30 mg/dl, when a year ago it was negative. 
He had blood in the urine at 50 Ery/μL when he has only had minor amounts before-due to taking a sample with the needle.
He had 1 Billirubin mg/dl when last year it was negative
He had Urobilinogen 4 mg/dl when last year it was normal
He had Red Cell count 22 /HPF when last year it was 1. 

His bloodwork:
Cobalamine: >1000-Determines if he's absorbing nutrients; might indicate IBD or disease/cancer if higher. The vet thought this was fine but the specialist thought it was too high.
Folate-16.5 ug/L-normal and if not might indicate IBD or disease/cancer.
PLI-pancreatic lipase-test for pancreatitis or cancer-1.9 ug/L-normal
Phos-4.9 up from 3.9 last year
Calcium 11.2 up from 9.3 last year
Albumin 4.1 up from 3.5 last year
ALT 194 up from 48 last year
Fructosamine 209 up from 175 in 2014-steadly climbing in the last four years
(The remainder of the CBC/CHEM panel was normal.)
Vitamin D-is high at 162 (normal is 150)
Cancer marker test:
TK1-5.1-too high would be over 7.5
f-HPT-43.3-normal range, too high would be over 64.9
Neoplasia Index-2.1-normal, too high would be over 5.5.
With the high normal TK1, they assume pancreatitis which matches the ultrasound findings.


His ultrasound:
"Bladder-...small...normal wall thickness, few hyperechoic floating particles in lumen consistent with cellular clumping as previously noted. No masses or calculi.
Kidneys-...Diffuse hyperechoic change to parenchyma...Mild blunting of calices...
Spleen-Normal in size. Diffusely hyperechoic, homgeneous parenchyma. Normal vascular pattern.
GI-...normal muscosal thickness...no mass....
Pancreas-...R limb prominent with mild mottling...Focal hyperechoic change and tissue thickening seen in mesentery associated with R limb.
Liver-Normal...homogeneous parenchyma with slight bulge to the capsule...
Other-No lymphadenopathy

Findings...fairly similar to those from (last year)...cellular clumping...bladder most consistent with mild hematuria. Kidneys...very mild scarring or low grade nephritis (as last year.)
Open etiology for the hematuria. FLUTD/FIC may be etiology for hematuria and intermittent inappropriate urination...mild, chronic pancreatic inflammation and scarring and mild subclinical hepatic lipidosis. Past vomiting 11/2019 may have occurred...bout of pancreatitis. Care must be taken to avoid high fat diets that may precipitate pancreatic inflammation.

*(She noted that the cobalamin was high. The regular vet said it was fine.)
Serum B12...consider decreasing or discontinuing supplementation if still being administered.
*(She suggested antibiotics even though no UTI was noted in urine. The vet said no to antibiotics without an issue showing up in blood or urine.)
Consider antibiotic trial with recheck UA to see if hematuria improves...
Ideally limit diets to low fat diets...W/D, I/D..."

The high cobalamin noted by the vet could be hypercobalaminaemia. In humans it is associated with hepatic and neoplastic disorders and the same might be present in cats. Here is one study:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4236818/

"In humans, hypercobalaminaemia is associated with myeloproliferative disorders and with a wide range of solid neoplasms including liver, mammary, prostatic, pulmonary, gastric and pancreatic tumours. It has, therefore, been suggested to be a non-specific marker for cancer. Associations have also been made with various non-neoplastic liver diseases and with kidney disease in some studies. To date, its significance has not been investigated in veterinary species. Therefore, the aim of this study was to determine whether disease associations exist for hypercobalaminaemia in cats.

...Among the remaining 156 cats with cobalamin measurement, complete medical records available, and no history of cobalamin supplementation, the serum cobalamin was greater than the reference interval in 44 ...Of the 33 hypercobalaminaemic cats with a definitive diagnosis, 15 were diagnosed with neoplasia, and 8 were diagnosed with non-neoplastic liver disease. Of the 15 hypercobalaminaemic cats with neoplastic disease, liver involvement was confirmed in 5 cases (2 cats with lymphoma, one cat with a metastatic splenic plasma cell tumour, one cat with a pancreatic carcinoma and one with a biliary cystadenoma)...Therefore, the current assumption that hypercobalaminaemia does not have clinical significance in veterinary species should be questioned, and prospective studies should be considered to confirm these preliminary findings...Hypercobalaminaemic cats in this study were also more likely to be diagnosed with liver disease, and similar associations are seen in humans...Possible mechanisms include leakage into the circulation following hepatocellular injury and impaired hepatic uptake of cobalamin. An association with hepatocellular injury is less likely, given that there was no correlation between serum ALT activity and cobalamin concentration. The association between hypercobalaminaemia and hepatobiliary disease in cats is intriguing, since hepatobiliary disease is also associated with hypocobalaminaemia...This discrepancy might reflect the tendency for concurrent gastrointestinal, pancreatic and hepatobiliary pathology in cats, having counteracting effects on serum cobalamin. Indeed, only 9 of the 17 hypercobalaminaemic cats with confirmed liver disease in this study had a disease confined to the hepatobiliary system. Alternatively, it could reflect differing effects of specific hepatobiliary diseases on cobalamin metabolism...there are effects on cobalamin metabolism as a result of changes in hepatic function caused by the PVH..."

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